Relevant bibliographies by topics / BCL2L1

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'BCL2L1'

Author: Grafiati
Published: 4 June 2021
Last updated: 13 February 2022

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Journal articles on the topic "BCL2L1"

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Haferlach, Claudia, Wencke Walter, Alexander Höllein, et al. "Identification and Characterization of Potential Candidates for Treatment Targeting Apoptosis Pathways in Patients with Hematological Neoplasms." Blood 132, Supplement 1 (2018): 4098. http://dx.doi.org/10.1182/blood-2018-99-117927.

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Abstract Background: Resistance to apoptosis is one of the hallmarks in hematological neoplasms, most typically via dysregulation of the intrinsic mitochondrial pathway. The most important antiapoptotic/pro-survival proteins in this pathway are BCL2, BCL2L1 and MCL1. Molecules targeting each of these proteins are in various stages of preclinical and clinical development. The BCL2 inhibitor venetoclax is the first FDA approved drug in this setting and was shown to be highly effective in CLL and some B-cell lymphoma subtypes. Kumar et al. (Blood 2017) reported that in multiple myeloma response t
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Handschuh, Luiza, Pawel Wojciechowski, Maciej Kazmierczak, and Krzysztof Lewandowski. "Transcript-Level Dysregulation of BCL2 Family Genes in Acute Myeloblastic Leukemia." Cancers 13, no. 13 (2021): 3175. http://dx.doi.org/10.3390/cancers13133175.

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The expression of apoptosis-related BCL2 family genes, fine-tuned in normal cells, is dysregulated in many neoplasms. In acute myeloid leukemia (AML), this problem has not been studied comprehensively. To address this issue, RNA-seq data were used to analyze the expression of 26 BCL2 family members in 27 AML FAB M1 and M2 patients, divided into subgroups differently responding to chemotherapy. A correlation analysis, analysis of variance, and Kaplan-Meier analysis were applied to associate the expression of particular genes with other gene expression, clinical features, and the presence of mut
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Türkmen, Seval, Mathias Riehn, Stefan Mundlos, Eckhard Thiel, and Thomas Burmeister. "A Novel BACH2-BCL2L1 Fusion Gene in the Burkitt’s Lymphoma Derived Cell Line BLUE-1." Blood 112, no. 11 (2008): 4146. http://dx.doi.org/10.1182/blood.v112.11.4146.4146.

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Abstract Abnormalities of the long arm of chromosome 6 are a common feature in various B-cell malignancies. However, in most cases the involved genes have not yet clearly been identified. We have molecularly characterized the recently established cell line BLUE-1 that has been derived from a relapsed sporadic Burkitt lymphoma. This cell lines carries a t(6;20)(q15;q11.2) rearrangement in addition to the typical t(8;14) with MYC-IgH fusion. The involved gene loci on chromosomes 6 and 20 were up to now unknown. To identify the involved gene loci on both chromosomes we applied a sequential BAC cl
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Jie, Yanghua, Xiaobei Yang, and Weidong Chen. "Expression and gene regulation network of TYMS and BCL2L1 in colorectal cancer based on data mining." PeerJ 9 (June 2, 2021): e11368. http://dx.doi.org/10.7717/peerj.11368.

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Background The purpose of this study was to study the role of thymidylate synthetase (TYMS) and B-cell lymphoma-2 like 1 (BCL2L1) in the occurrence and development of colorectal cancer and its potential regulatory mechanism. Methods The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) were analyzed to examine the expression and prognostic value of TYMS and BCL2L1 in colorectal cancer. C-BioPortal analysis was used to detect the TYMS and BCL2L1 alterations. Through The Human Protein Atlas (THPA), the TYMS and BCL2L1 protein levels were also assessed. The protein protein interaction
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Park, Hansoo, Sung-Yup Cho, Hyerim Kim, et al. "Genomic alterations in BCL2L1 and DLC1 contribute to drug sensitivity in gastric cancer." Proceedings of the National Academy of Sciences 112, no. 40 (2015): 12492–97. http://dx.doi.org/10.1073/pnas.1507491112.

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Gastric cancer (GC) is the third leading cause of cancer-related deaths worldwide. Recent high-throughput analyses of genomic alterations revealed several driver genes and altered pathways in GC. However, therapeutic applications from genomic data are limited, largely as a result of the lack of druggable molecular targets and preclinical models for drug selection. To identify new therapeutic targets for GC, we performed array comparative genomic hybridization (aCGH) of DNA from 103 patients with GC for copy number alteration (CNA) analysis, and whole-exome sequencing from 55 GCs from the same
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Kelly, Jennifer L., Anne J. Novak, Zachary S. Fredericksen, et al. "Germline Variation in Apoptosis Pathway Genes and Risk of Non-Hodgkin Lymphoma." Blood 114, no. 22 (2009): 3933. http://dx.doi.org/10.1182/blood.v114.22.3933.3933.

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Abstract Abstract 3933 Poster Board III-869 Background Non-Hodgkin Lymphoma (NHL) is a malignancy of lymphocytes with few known risk factors identified to date. Members of the BCL2 and caspase gene families are known regulators of programmed cell death in these cells, and the t(14;18)(q32;q21) is the most commonly observed chromosomal translocation in NHL, a somatic event which results in constitutive BCL2 expression and inhibition of apoptosis. Further, recent pooled analyses of three case-control studies reported gene level associations for both BCL2L11 (Cancer Epidemiol Biomarkers Prev 2009
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Cleynen, Alice, Mehmet Samur, Aurore Perrot, et al. "Variable BCL2/BCL2L1 ratio in multiple myeloma with t(11;14)." Blood 132, no. 26 (2018): 2778–80. http://dx.doi.org/10.1182/blood-2018-09-876433.

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Castillo-Martín, Miriam, Marc Yeste, Eva Pericuesta, Roser Morató, Alfonso Gutiérrez-Adán, and Sergi Bonet. "Effects of vitrification on the expression of pluripotency, apoptotic and stress genes in in vitro-produced porcine blastocysts." Reproduction, Fertility and Development 27, no. 7 (2015): 1072. http://dx.doi.org/10.1071/rd13405.

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The aims of the present study were to: (1) evaluate the effect of vitrification and warming on quality parameters and expression levels of pluripotency, apoptotic and stress genes in in vitro-produced (IVP) porcine blastocysts; and (ii) determine the correlation between these parameters. To this end, total cell number, DNA fragmentation, peroxide levels and the relative transcript abundance of BCL-2 associated X protein (BAX), BCL2-like 1 (BCL2L1), heat shock protein 70 (HSPA1A), POU class 5 homeobox 1 (POU5F1), superoxide dismutase 1 (SOD1) and superoxide dismutase 2 (SOD2) were analysed in f
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Song, Chunhua, Zheng Ge, Yali Ding, et al. "IKAROS and CK2 regulate expression of BCL-XL and chemosensitivity in high-risk B-cell acute lymphoblastic leukemia." Blood 136, no. 13 (2020): 1520–34. http://dx.doi.org/10.1182/blood.2019002655.

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Abstract High-risk B-cell acute lymphoblastic leukemia (B-ALL) is an aggressive disease, often characterized by resistance to chemotherapy. A frequent feature of high-risk B-ALL is loss of function of the IKAROS (encoded by the IKZF1 gene) tumor suppressor. Here, we report that IKAROS regulates expression of the BCL2L1 gene (encodes the BCL-XL protein) in human B-ALL. Gain-of-function and loss-of-function experiments demonstrate that IKAROS binds to the BCL2L1 promoter, recruits histone deacetylase HDAC1, and represses BCL2L1 expression via chromatin remodeling. In leukemia, IKAROS’ function i
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Ramezani-Rad, Parham, Huimin Geng, Lai N. Chan, et al. "SOX4 enables Oncogenic Survival Signals in Acute Lymphoblastic Leukemia." Blood 120, no. 21 (2012): 863. http://dx.doi.org/10.1182/blood.v120.21.863.863.

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Abstract Abstract 863 Background: The SOX4 (SRY-related HMG-box) transcription factor is expressed in early B- and T- cell development. In the absence of SOX4, B cell development is arrested at the pro-B to pre-B cell transition. In Sox4−/− mice, pro-B cells fail to proliferate in response to IL7 and to expand and differentiate past the pre-B cell receptor checkpoint. Interestingly, SOX4 functions a transcription factor yet closely interacts with membrane-proximal cytokine receptor signaling. The PDZ domain-containing adaptor protein syntenin (SDCBP) recruits the Sox4 protein directly to the c
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Dissertations / Theses on the topic "BCL2L1"

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Ismail, Jaidaa. "Testing BCL2A1 Small Molecule Inhibitors in Fluorescence Polarization Assays." University of Cincinnati / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1595846503840908.

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Lionnard, Loïc. "Régulation de la stabilité de la protéine anti-apoptotique BCL2A1." Thesis, Montpellier, 2018. http://www.theses.fr/2018MONTT003/document.

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L’apoptose ou mort cellulaire programmée joue un rôle prépondérant dans l’homéostasie cellulaire. Ce processus est très finement régulé par les protéines de la famille BCL-2 qui contrôlent la perméabilité de membrane mitochondriale externe et la libération du cytochrome c, deux événements majeurs précédant la mort cellulaire. Les protéines anti-apoptotiques de la famille BCL-2 contribuent à la tumorigenèse et sont impliquées dans la résistance des cancers aux molécules chimiothérapeutiques ; à ce titre, elles représentent des cibles importantes pour le développement de nouvelles thérapies. BCL
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Nougarede, Adrien. "Molecular basis of BCL2L10/Nrh oncogenic activity in breast cancer." Thesis, Lyon, 2016. http://www.theses.fr/2016LYSE1192/document.

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L'apoptose, ou « mort cellulaire programmée », joue un rôle clé dans de nombreux processus biologiques. Les protéines de la famille Bcl-2, dont l'expression est souvent altérée dans les cellules tumorales, sont les principaux régulateurs de l'apoptose. Parmi cette famille, la fonction exacte du répresseur apoptotique Nrh, aussi appelé BCL2L10 ou Bcl-B, reste à ce jour mal comprise. Bien que son expression ne soit pas détectable dans la plupart des tissus sains, on retrouve des niveaux élevés de Nrh corrélés à un mauvais pronostique dans les cancers du sein et de la prostate. Nous avons mis au
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Jenal, Mathias. "HIC1 and BCL2A1 : novel factors involved in myeloid differentiation and survival /." Bern : [s.n.], 2009. http://www.zb.unibe.ch/download/eldiss/09jenal_m.pdf.

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Shipanga, Hendrina. "The role of BCLFA1 in cellular transformation." Master's thesis, University of Cape Town, 2018. http://hdl.handle.net/11427/29307.

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The malignant transformation of normal cells into cancer cells result in the loss of control of cellular regulatory mechanisms such as loss of function of tumour suppressors and gain of function of oncogenes. Genetic mutations may be inherited or acquired during the process of malignant transformation, such that the normal mechanisms responsible for control cellular proliferation become dysfunctional. Aberrations of the BCLAF1 gene located on chromosome 6q23 has previously been detected by whole genome sequence analysis of DNA from oesophageal cancer biopsies. Although the role of BCLAF1 is no
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Thorman, Alexander W. "Rational Design of Novel BCL2A1 Inhibitors for Treatment of Autoimmune Diseases: An Integration of Virtual Screening, Transcriptomics and Protein Biophysics." University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1543580409766192.

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Molitoris, Jason K. "Mechanistic Insights into Glucocorticoid-induced Apoptosis and Autophagy in Lymphoid Malignancies." Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1307646327.

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Lee, Song Choon. "Characterisation of Bcl11 functions in development using genetically modified mice." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611189.

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Rech, de Laval Valentine. "Analyse bioinformatique des protéines BCL-2 et développement de la base de connaissance dédiée, BCL2DB." Thesis, Lyon 1, 2013. http://www.theses.fr/2013LYO10273/document.

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Les protéines BCL-2 jouent un rôle essentiel dans la décision de vie ou de mort des cellules. Elles contrôlent l'induction de l'apoptose (mort cellulaire programmée) par la voie mitochondriale via des fonctions opposées de régulateurs anti- et pro-apoptotiques. Les protéines contenant un ou plusieurs domaines dits d'homologie à Bcl-2 (BHl- 4) sont systématiquement classées dans cette famille. Grâce à une analyse bioinformatique et phylogénétique, nous avons revisité les différents critères d'inclusion dans le groupe de protéines BCL-2 et proposé une nouvelle classification tenant compte des do
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Leal, Cristina Tavares. "Identificação da família BCL2 como alvo terapêutico no tratamento das neoplasias mieloproliferativas associadas à mutação da JAK2V617F." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/17/17154/tde-06042018-114114/.

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As neoplasias mieloproliferativas (NMPs) negativas para o rearranjo t(9;22)/BCRABL1, incluindo Policitemia Vera (PV), Trombocitemia Essencial (TE) e Mielofibrose Primária (MFP), são doenças hematopoéticas clonais e estão frequentemente associadas à mutação JAK2V617F. Apesar dos avanços no conhecimento da fisiopatologia após a descoberta da mutação JAK2V617F e do desenvolvimento de inibidores da JAK2, o tratamento permanece não curativo. Sabe-se que as célulastronco mais primitivas nas NMPs são responsáveis pela iniciação da doença e que a expansão dos precursores mieloeritróides contribui para
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Books on the topic "BCL2L1"

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Ward, Mary A. Robert Elsmere (Bcl1-Pr Eng Lit Ser). Reprint Services Corp, 1996.

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Byron, Byron George Gordon, and John C. Fox. The Byron Mystery (Bcl1-Pr English Literature). Reprint Services Corporation, 1992.

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Brooks, Van Wyck. Emerson and Others (Bcl1-Ps American Literature). Reprint Services Corp, 1992.

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Fausset, Hugh I'anson. Samuel Taylor Coleridge (BCL1-PR English Literature). Reprint Services Corp, 2007.

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Melville, Herman. Encantadas: Or Enchanted Isles (Bcl1-Ps American Literature). Reprint Services Corporation, 1993.

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Hetz, Claudio. BCL2 Protein Family: Essential Regulators of Cell Death. Springer, 2011.

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Adams, Leonie. Those Not Elect (Bcl1-Ps American Literature Ser.). Reprint Services Corp, 1992.

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Sinclair, May. The Three Brontes (Bcl1-Pr English Literature Series). Reprint Services Corp, 1992.

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Siebert, Wilbur Henry. Underground Railroad from Slavery to Freedom (Bcl1 U.S. History). Reprint Services Corp, 1992.

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Cerf, Vinton G. Modern American Short Stories (Bcl1-Ps American Literature Series). Reprint Services Corp, 1993.

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Book chapters on the topic "BCL2L1"

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Saidak, Zuzana, Zakaria Ezzoukhry, Jean-Claude Maziere, et al. "BCL-XL, BCL2L, BCL2L1 (BCL-2 Like 1)." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100114.

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Saidak, Zuzana, Zakaria Ezzoukhry, Jean-Claude Maziere, et al. "BAX (BCl2-Associated X Protein), BCL2L4 (BCL-2 Like 4)." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100109.

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Biswas-Fiss, Esther E., Stephanie Affet, Malissa Ha, et al. "A1 (BCL2-Related Protein A1), BFL-1, BCL2L5 (BCL-2 like 5)." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100023.

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Saidak, Zuzana, Zakaria Ezzoukhry, Jean-Claude Maziere, et al. "BAD (BCL-2-Associated Agonist of Cell Death), BBC6 (BCL2-Binding Component 6), BCL2L8 (BCL2-Like Protein 8)." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100104.

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Saidak, Zuzana, Zakaria Ezzoukhry, Jean-Claude Maziere, et al. "BCL-W, BCL2L2 (BCL-2 Like 2)." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100113.

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Ruggiero, Marco. "Bcl2." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_562.

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Ruggiero, Marco, and John W. Anderson. "Bcl2." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_562-4.

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Ruggiero, Marco, and John W. Anderson. "Bcl2." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-642-27841-9_562-5.

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Ruggiero, Marco, and John W. Anderson. "Bcl2." In Encyclopedia of Cancer. Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_562.

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Saidak, Zuzana, Zakaria Ezzoukhry, Jean-Claude Maziere, et al. "BAK (BCL-2 Antagonist Killer), BCL2L7 (BCL-2 Like 7), CDN1." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100106.

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Conference papers on the topic "BCL2L1"

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Rajagopal, N., G. Hodgson, S. Hu, et al. "Abstract P1-09-08: BCL2L1 (BCL-XL) expression and MYC super-enhancer positivity predict sensitivity to the covalent CDK7 inhibitor SY-1365 in triple negative breast cancer (TNBC) cell lines." In Abstracts: 2017 San Antonio Breast Cancer Symposium; December 5-9, 2017; San Antonio, Texas. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.sabcs17-p1-09-08.

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ohtsu, Akira, Seiji Arai, Tatsuhiro Sawada, and Kazuhiro Suzuki. "Abstract 1928: Erdafitinib in combination with BCLXL/BCL2 inhibitor induce apoptosis in urothelial carcinoma cells without FGFR mutation." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1928.

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Jensen, Samuel A., Andrea Calvert, Janina Luciano, and Alexander Stegh. "Abstract 2005: Identification of Bcl2L13 as a novel GBM oncoprotein." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2005.

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Kouri, Fotini M., Yongfei Wu, Lynda Chin, and Alexander H. Stegh. "Abstract 1107: MicroRNA-182 acts as a chemosensitizer in GBM by repressing Bcl2L12." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1107.

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Kladi-Skandali, Athina, Christos K. Kontos, Alexandros Tzovaras, et al. "Abstract LB-72: Expression of theBCL2-like 12(BCL2L12) gene is associated with prolonged survival of breast adenocarcinoma patients." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-lb-72.

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Haile, Lydia, Jose Medina Echeverz, Fei Zhao, et al. "Abstract 467: Bcl2A1 - an IFN-gamma dependent master switch for the function of CD11b+Gr-1high myeloid derived suppressor cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-467.

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Mestanza, Jéssica, Yenddy Carrero, and Núñez Iveth. "Expresión de BAX y BCL2 en lesiones cervicales." In V Congreso Internacional de Investigación en Ciencias de la Salud y II Seminario Internacional de Nutrición y Salud Alimentaria. Medwave, 2021. http://dx.doi.org/10.5867/medwave.2021.s1.cs25.

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Lopez-Garcia, Carlos, Nicholas McGranahan, Sebastjian Hobor, et al. "Abstract 3584: Genomic analysis reveals a role for BCL9L in aneuploidy tolerance in colorectal cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3584.

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Zapata, Claudia, Jorida Coku, Kangning Liu, et al. "Abstract 2504: Predictive biomarkers for Bcl2-inhibitor use in neuroblastoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2504.

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Moses, Blake S., Jennifer M. Fox, Xiaochun Chen, et al. "Abstract 2023: Artemisinins enhanced the antileukemic efficacy of BCL2 inhibitors." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2023.

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Reports on the topic "BCL2L1"

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Baker, William C. Racial Differences in Prostate Cancer Molecular Biology: An Evaluation of Tumor Suppressor Genes in BCL2, P53 and RB in Black and Africans. Defense Technical Information Center, 1999. http://dx.doi.org/10.21236/ada376157.

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